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EC number: 254-413-8 | CAS number: 39318-18-8
- The addition of 250 ppm sodium tungstate had little or no effect on the xanthine dehydrogenase activity of the hen tissues tested.
- 500 ppm tungsten caused a steady decline in xanthine dehydrogenase activity, which appeared to stabilize around 30 days.
- Neither level of sodium tungstate had an apparent effect on the rate of egg production or hatchability.
Experiment 2, Trial 1 and Trial 2
-Day old chicks from hens fed tungstate had significantly higher amounts of xanthine dehydrogenase in the liver and intestine than did chicks from hens receiving no tungstate.
- Chicks from hens fed the tungsten-supplemented ration grew at a significantly slower rate than did the control chicks on both the breeder ration and the broiler ration.
- When the chick ration was supplemented with 500 ppm tungsten, a slower rate of gain was observed when compared to rations containing no supplementation.
- At four weeks of age, there appeared to be no difference in the xanthine dehydrogenase activities between the chicks, regardless of the ration fed or the hen treatment
-The variation that occurred in the enzyme determinations was large, and the sample size relatively small. This may have accounted for there being no statistical differences.
No bird toxicity data of sufficient quality are available for tungsten oxide (target substance). However, bird toxicity data are available for sodium tungstate (source substance), which will be used for reading across. Due to lower water solubility and lower toxicity for the target substance compared to the source substance, the resulting read across from the source substance to the target substance is appropriate as a conservative estimate of potential toxicity for this endpoint. In addition, read across is appropriate because the PBT/vPvB profile is the same, and the dose descriptors are, or are expected to be, lower for the source substance. For more details, refer to the read-across category approach included in the Category section of this IUCLID submission and/or as an Annex in the CSR.
Table 2. Effects of diets containing W on growth and xanthine dehydrogenase activities of chicks.
Xanthine dehydrogenase (XD) activity (mm302/20 min/flask), week 6
Group 1: base diet:
Group 2: base diet with trace amounts of molybdenum
Group 4: 45 mg/kg tungsten
Group 8: 94 mg/kg tungstent
XD levels measured after 6 weeks on the diets, using 28.3 mg liver or kidney, and 84.9 mg intestine or pancreas per flask.
- After 3 weeks, 6 chicks from Groups 8 (94 mg/kg W) were sacrificed, and analyzed for Xanthine dehydrogenase and Mo.
- The mean values for intestine, liver, kidney, and pancreas were 0.4, 2.2, 0.2, and 0.8 mm3O2/20 min. respectively for Group 8 (avg Mo 0.20 ug/g dry wt)
- Therefore, within 3 weeks, the addition of 94 mg/kg to the diet markedly depressed tissue Mo and XD activities.
- After 6 weeks, half of the uric acid normally produced by chicks was replaced by a mixture of xanthine and hypoxanthine in Group 8.
Liver molybdenum concentrations and the activity of liver xanthine dehydrogenase were markedly reduced only when the tungsten concentration of tissues approached this high concentration.
The proportion of the liver molybdenum contributing to the xanthine dehydrogenase enzyme was calculated for experiment 2 from the known specific activity of highly purified extracts of this enzyme from chicken and turkey liver These calculations indicated that at normal liver molybdenum concentrations approximately 37% of the liver molybdenum was bound to xanthine dehydrogenase, while at the lowest molybdenum concentrations observed prior to death (seen in injection groups only) only approximately 7% of the liver molybdenum was bound to the enzyme. This would suggest that these chicks were affected primarily by a tungsten toxicity rather than by a simple molybdenum deficiency.
Several older studies on chicken species were identified in which the birds were fed varying amounts of tungsten, in the form of sodium tungstate in their diets. The NOAELs identified from these studies ranged from approximately 45-500 mg tungsten/kg, depending on which endpoints were examined in each study. However, none of these studies were conducted with standard methodology and they were deemed to be less than reliable. Therefore, they will not be used directly to calculate the PNEC oral.
Due to similar or lower transformation/dissolution results for tungsten blue oxide (the target substance) than sodium tungstate (the source substance), the resulting toxicity potential would also be expected to be similar or lower, so read-across is appropriate. In addition, read-across is justified because the classification and labelling is the same or less severe for the target substance PBT/vPvB profile is the same. Finally, the dose descriptors are, or are expected to be, sufficiently similar or higher for the target substance, and read-across to the source chemical is adequately protective. For more details refer to the attached description of the read across approach.
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